Innate immune responses and chronic obstructive pulmonary disease: "Terminator" or "terminator 2"?

Robert P. Schleimer*

*Corresponding author for this work

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

Innate immune responses appear to be partially responsible for maintaining inflammation and tissue destruction in chronic obstructive pulmonary disease. In the early stages of the disease in smokers, the airways are bombarded with large quantities of participate material, and activation of phagocytic cells results in the release of many of the mediators believed to remodel the airways. Ironically, failure of the innate immune defense system, either by inherited deficiency or as a result of chronic smoke inhalation, is likely to result in increased susceptibility to infectious disease and exacerbations of chronic obstructive pulmonary disease. It is well known that deficiencies in the production of collectins, pentraxins, and complement can lead to increased infections, and several studies indicate that deficiency in one or another innate defense component is associated with increased exacerbations. Corticosteroids reduce exacerbations in part because of their ability to boost the production of innate host-defense molecules. Therapeutic approaches that stimulate the generation of antimicrobial molecules in the lungs might be able to reduce disease exacerbations.

Original languageEnglish (US)
Pages (from-to)342-346
Number of pages5
JournalProceedings of the American Thoracic Society
Volume2
Issue number4
DOIs
StatePublished - 2005

Keywords

  • Acute phase responses
  • Corticosteroids
  • Exacerbations
  • Inflammation
  • Opsonins

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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